Evidence map›Paper›PMID 30955235›Full record

ArticleCancer science2019

MicroRNA-331-3p inhibits epithelial-mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β-catenin axis in non-small-cell lung cancer.

Xizhe Li, Jiali Zhu, Yuanqi Liu, Chaojun Duan, Ruimin Chang, Chunfang Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.7field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 66 citations in OpenAlex.

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  4. [Research Progress of Engineered Exosomes in the Treatment of Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Xizhe LiDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, China.ORCID https://orcid.org/0000-0003-1852-1894
Jiali ZhuDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, China.
Yuanqi LiuDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, China.
Chaojun DuanInstitute of Medical Sciences, Key Laboratory of Cancer Proteomics of Chinese Ministry of Health, Xiangya Hospital, Central South University, Changsha, China.ORCID https://orcid.org/0000-0001-5349-7725
Ruimin ChangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, China.
Chunfang ZhangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, China.
Central South University · CN

Funding

National Natural Science Youth Foundation of China 81602027Natural Science Foundation General Program of Hunan Province 2018JJ3821Project of Scientific Research Plan of Hunan Provincial Health Commission C2019185Youth Foundation of Xiangya Hospital Central South University 2015Q01
6 · The paper itself

Abstract

MicroRNAs have been reported to play critical roles in the regulation of non-small-cell cancer (NSCLC) development, but the role of microRNA (miR)-331-3p in NSCLC is still unclear. In this study, the expression levels of miR-331-3p in NSCLC tumor tissues and adjacent normal tissues were examined by quantitative RT-PCR, and the relationship between miR-331-3p expression and patient clinicopathological characteristics was analyzed. The effects of miR-331-3p on epithelial-mesenchymal transition (EMT), migration, and metastasis of NSCLC cells were determined in vitro and vivo. Direct functional targets of miR-331-3p were identified by luciferase reporter assay, western blot assay, immunohistochemical staining, and rescue assay. The downstream pathway regulated by miR-331-3p was identified by immunofluorescence, immunoprecipitation, and Rac1 activity examination. Our results showed that miR-331-3p was significantly downregulated in NSCLC tumor tissues and was correlated with clinicopathological characteristics, and miR-331-3p could be an independent prognostic marker for NSCLC patients. Furthermore, miR-331-3p significantly suppressed EMT, migration and metastasis of NSCLC cells in vitro and in vivo. Both ErbB2 and VAV2 were direct functional targets of miR-331-3p. The activities of Rac1, PAK1, and β-catenin were regulated by miR-331-3p through ErbB2 and VAV2 targeting. These results indicated that miR-331-3p suppresses EMT, migratory capacity, and metastatic ability by targeting ErbB2 and VAV2 through the Rac1/PAK1/β-catenin axis in NSCLC.

Indexed as

Gene Expression Regulation, NeoplasticA549 Cellsbeta CateninCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionErb-b2 Receptor Tyrosine KinasesFemaleHumansLung NeoplasmsMaleMicroRNAsMiddle Agedp21-Activated KinasesProto-Oncogene Proteins c-vavbeta CateninERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesMicroRNAsMIRN331 microRNA, humanp21-Activated KinasesPAK1 protein, humanProto-Oncogene Proteins c-vavrac1 GTP-Binding ProteinVAV2 protein, humanErbB2microRNAnon-small-cell lung cancerRac1VAV2

Identifiers

PMID30955235
PMCPMC6550127
OpenAlexW2930915742

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.